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Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1 Case 1 A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago

4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs. 2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles. 4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed

at night since then and has slept on 3 pillows. Yesterday, he became breathless walking from one room to another He presents today with extreme shortness of breath He denies chest pain BP 108/52 P 140, irreg. R 30 and labored Temp 99F Ht: 5'8"

Wt: 210. General: Breathless, moderately obese male in acute distress sitting upright complaining "I am going to die. Please help me." Chest: Scattered rhonchi throughout, rales bilateral one third lower bases. Cough is productive and frothy. CVS: Tachycardia and irreg. Grade 3/6 systolic murmur at LSB, S3 gallop noted. JVP to jaw Abd: Liver palpable three centimeters below right costal margin. HJR. Extremities: 4+ pitting edema of lower extremities to the knees. Pulses intact.

Organization of CHF Importance Pathophysiology Diagnosis Etiologies Decompensation Management Cardiomyopathy Importance Increasing burden

Aging population Improved survival (Hypertension/CAD) Nationwide, heart failure affects more than 400 000 Canadians1 (10% of those >75) >50 000 new cases are diagnosed /yr1 Bad Disease Mortality

1 year 10-20% 6 year 60-80% ED visits 20% new diagnosis 80% repeat visit (decompensation) Definition CHF Inability of the heart to maintain adequate vital organ perfusion at normal filling pressures

Decreased exercise capacity Associated neurohumoral-endocrine changes, initially compensatory but ultimately maladaptive Pulmonary Edema A condition associated with increased loss of fluid from the pulmonary capillaries into the pulmonary interstitium and alveoli The heart is a pump that works together with the lungs. It pumps

blood in 2 ways 1. It pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heart 2. It then pumps blood out into the circulatory system of blood vessels that carry blood through the body In HF the pumping action of the heart becomes less and less efficient/powerful The heart does not pump blood as well as it should

When this happens, blood does not move efficiently through the circulatory system It starts to back up, increasing the pressure in the blood vessels, forcing fluid from the blood vessels into body tissues. Physiology CO = HR X Stroke Volume SV = preload + contractility - afterload Preload

initial stretching of the cardiac myocytes prior to contraction Afterload the "load" that the heart must eject blood against Aortic pressure Stroke Volume Hypertrophy is a mechanism that allows more muscle fibers to share the work

Contractility ability of a cardiac muscle fiber to contract at a given fiber length catecholamines (norepi and epi) sympathetic stimulation Ca++ Neurohormonal Activation Jackson, G et al. BMJ 2000;320:167-170

Copyright 2000 BMJ Publishing Group Ltd. [Nor-epi] and Mortality Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. Sympathetic Activation

Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. Remodelling Post MI Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. Classification of Heart

Failure Low Output Cardiac output is low, but demand for blood flow is normal The heart is unable to meet this demand and fails Dx: IHD, HTN, dilated cardiomyopathy, valvular and pericardial dz High Output High-output heart failure Cardiac output is normal or a little bit high Demand for blood flow is abnormally high (hyperthyroidism, anemia, severe infections)

The heart is unable to deliver the increased amount of blood and fails Dx: hyperthyroidism, anemia, pregnancy, AV fistulas, beriberi, & Pagets Rx: volume overload and correct the underlying disorder Classification of Heart Failure Acute MI, Acute Valve Dysfunction

largely systolic sudden reduction in cardiac output often results in systemic hypotension without peripheral edema Chronic Cardiomyopathy arterial pressure tends to be well maintained until very late in the course there is often accumulation of peripheral edema

Classification of Heart Failure Right Sided (right ventricle) (pulmonic stenosis or pulmonary hypertension) When the right side of the heart starts to fail, fluid collects in the feet and lower legs As the heart failure becomes worse, the legs swell and eventually the abdomen collects fluid (ascites, hepatic congestion) Weight gain accompanies the fluid retention and is an

excellent measure of how much fluid is being retained. Left Sided (left ventricle) left ventricle is mechanically overloaded (aortic stenosis) or weakened (post MI) When the left side of the heart starts to fail, fluid collects in the lungs (Orthopnea/PND) Breathing becomes more difficult, and the patient may feel short of breath, particularly with activity or lying down This extra fluid in the lungs makes it more difficult for the

airways to expand on inhalation O2 diffusion Classification of Heart Failure Systolic The heart has difficulty contracting and pumping out enough blood weakness, fatigue and decreased ability to exercise

Ejection fraction = (stroke volume)/(end diastolic volume) A normal ejection fraction is greater than 50% Systolic heart failure has a EF < 50%. Diastolic The heart is unable to fill properly during diastole filling pressure This impedes blood filling into the heart backup into

the lungs CHF symptoms in patients > 75 years; women; HTN Ejection fraction is normal Classification of Heart Failure Directional Heart Failure Backwards heart failure The ventricle is not pumping out all the blood that comes into it. ventricular filling pressure and systemic or pulmonary edema

In fact, the heart can only meet the needs of the body if the ventricular filling pressure is high Forward heart failure The heart is not pumping out enough blood to meet the needs of the body blood reaches the kidneys, they conserve salt and water, which contributes to excess fluid retention and edema Forward failure also decreases the blood flow to various organs, causing weakness and fatigue

Diagnosis History Phsyical EKG CXR History Prior Heart Dz, Dyspnea, PND, Orthopnea, Fatigue, Cough, Bloating, Angina, Wt/Girth, Nocturia

Precipitants salt, non-compliance, new meds, NSAIDs, palpitations, angina Comorbidities (COPD, Renal Dz, DM) PE

HR RR JVP HJR Precordial exam: Apical impulse Location, Size, Sustained (45 LLD position exp)

Loud P2 S3 (ventricular vibration with rapid filling) Low pitched (bell) 45 LLD position Lungs: Cracks / Wheezes Peripheral Edema Case 2

58 F with known Idiopathic Dilated Cardiomyopathy Cardiac Cath (05): N coronaries LVEF 35% Meds: ACE-I, Diuretics, Digoxin SOBOE x 3weeks OE: Displaced MPI Soft S3 Pre-sacral edema Case 3 70 M Obese

SOBOE and fatigue x 3 months No Orthopnea/PND PMHx: Smoke x 40 pack-years, HTN (poorly controlled) DMII OE: BP 180/100 Sustained MPI Bilateral Rales Mild/Moderate Pretib Edema X-ray

Cardiomegally LV or hypertrophied ventricular wall Cardiothoracic Ratio > 50% Redistribution (cephalization) Systolic dys-fxn filling pressure Upper lobe vessels > Lower lobe vessels Blunting of costophrenic Angle Peribronchial cuffing Kerly-B lines

Peri-Bronchial Cuffing First, strike for the jugular and let the rest go! Oliver W. Holmes Jr. Etiology Dysrhythmia Tachy

Diastolic filling time +/- atrial kick CO Coronary perfusion Myocardial O2 demand Brady HR

CO = SV x HR Infection systemic met demands Pulm infection = O2 Tachycardia Anemia Isovolumic hemodilution CO meet O2 demands Coronary O2 delivery

Pregnancy demand for CO Acute Myocarditis contactility Acute valvular dysfunction 2o to MI preload or afterload

PE O2 supply Pulmonary Hypertension Pharmacologic inotropic effects Na / H2O retention Etiology Decompensation/Causes of exacerbation FAILURE:

25% Forgot medication Arrhythmia/ Anemia 10% Ischemia/ Infarction/ Infection (Pneumonia) Lifestyle: taken too much salt 25% Up-regulation of CO: pregnancy, hyperthyroidism Renal failure

Embolism: pulmonary 10% Inappropriate treatment 20% Failure to seek care Case 1 Management A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago

4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs. 2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles. 4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed at night since then and has slept on 3 pillows.

Yesterday, he became breathless walking from one room to another He presents today with extreme shortness of breath He denies chest pain Management Treat the maladaptation Vascular resistance Sympathetic tone Total blood volume

? LMNOP Management

Nitrates Nitrates Nitrates O2 Ventilation Assist Devices ACE I Diuretics Morphine Inotropes

Airway/Breathing Non-rebreather facemask delivering 100% O2 Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.

NIPPV If respiratory distress and/or hypoxia persist, consider non-invasive PPV preload, afterload, and left ventricular performance Meta-analysis of 15 clinical trials: mortality and intubation with NPPV compared to conventional therapy Patients who fail/do not tolerate/have contraindications to NPPV should be intubated Positive end-expiratory pressure is often useful for

improving oxygenation Multi-centre RCT

130 pts Cardiogenic Pulmonary Edema Emergency Department Medical therapy+O2 (65 pts) non-invasive pressure support ventilation (65 pts) Primary outcome need for intubation Loop Diuretics Na & H2O excretion Useful in volume overload Rapid onset

Mild vasodilator 1/2 life in CHF be careful Depletion of K + and Mg++ Loop Diuretics Dosing not well established High dose Lasix and low dose Nitro has worse outcomes than low dose Lasix and high dose Nitro

Morphine Controversial Weak vasodilator / Resp Drive ICU admisssions (OR = 3) Sacchetti ?Anxiolytic Nitrates preload @ low dose afterload @ high dose Nitrates - Route

SL/Spray (0.1 - 0.4mg / 5 min) x3 50-100ug/min IV Drip (5-10ug/min) titrate to effect (100-200ug) Transdermal Peripherally shut down Unreliable absorption

Contraindications / Cautions Viagra RV MI Fixed Aortic Lesions Case 4 67 M SOB Visibly Distressed 96 28 200/110 75% ORA PMHx: HTN, DM II EKG:

Nitroprusside Direct smooth muscle relaxant Balanced reduction of pre/after load Continuous pressure monitoring good Avoid hypotension Case 5 67 M SOB Visibly Distressed

96 28 140/90 75% ORA PMHx: HTN, DM II Meds: Inconsistent Natriuretic Peptide Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. Nesiritide

Recombinant BNP Aldosterone Endothelin Na & H2O excretion no reflex tachy Good for Nitro contraindications VMAC

Randomized, Double Blind 489 inpatients IV Nisiritide vs IV Nitrates vs Placebo PCWP and Dyspnea Improvement in PCWP 2mm HG @ 6h No change in Dyspnea Problems:

Nitro dosing Prolonged Hypotension Not ED patients Industry sponsored Vosodilator Therapy: Nesiritide Efficacy Phase

432 patients In the efficacy phase, 127 patients underwent hemodynamic monitoring with a pulmonary artery catheter A six hour infusion of nesiritide (0.015 and 0.03 g/kg per min) decreased pulmonary capillary wedge pressure (6 and 10 mmHg versus an of 2 mmHg for placebo) Improved the clinical status in a greater number of patients (60% and 67% versus 14%) Comparative phase

305 patients Randomly assigned to nesiritide or standard vasoactive agents for seven days without hemodynamic monitoring Compared to standard treatment with a single vasoactive agent (dobutamine, milrinone, nitroglycerin, or nitroprusside) nesiritide produced a similar significant improvement in clinical status and reduction in dyspnea and fatigue that persisted during the entire infusion period. Asymptomatic, dose-related hypotension was the most common side effect

Death within 30 days tended to occur more often among patients randomized to nesiritide therapy 35 [7.2%] of 485 vs 15 [4.0%] of 377 patients RR from meta-analysis: 1.74 (95% confidence interval [CI], 0.97-3.12; P = .059) Hazard ratio after adjusting for study, 1.80

(95% CI, 0.98-3.31; P = .057) Vasodilator Therapy Nitroglycerin: preload afterload Nitroprusside: afterload Nesiritide - BNP ACE Inhibitors Clear longterm benefits 1. 2.

3. 4. Vasodilate Block Aldosterone Bradykinin System Remodeling Take longer to work than nitrates (peak effect 45min)

Effect of ACE-I Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. Placebo-Controlled, Randomized, Double-Blind Study of Intravenous Enalaprilat Efficacy and Safety in Acute Cardiogenic Pulmonary Edema The purpose of this study was to evaluate the efficacy and safety of a single IV 2-hour infusion of enalaprilat (1 mg)

placebo-controlled, randomized, double-blind study 20 CHF patients (NYHA class III or IV) Compared with placebo, enalaprilat

pulmonary capillary wedge pressure (-37% versus -10%, P=.001), diastolic and mean systemic blood pressures (-21% vs 0%, P=.009, and -18% vs -1%, P=.026) diastolic and mean pulmonary blood pressures (-21% vs -8%, P=.040; -18% vs -9%, P=.046) brachial and renal resistances (-44% versus -14%, P=.017, and -22% versus -2%, P=.014) brachial and renal blood flows (+77% versus +8%, P=.036, and +12% versus 0%, P=.043) arterial oxygen tension (+2% versus -16%, P=.041)

arterial oxygen saturation (+1% versus -2%, P=.045) Enalaprilat did not affect CO or carotid or hepatosplanchnic hemodynamics Excluded those already on ACE I BNP Why do we need another diagnostic test? Diagnostic uncertainty

How uncertain are we? How uncertain should we be? ER docs are rarely wrong when they rate the probability of HF as very high or very low2 ER docs are uncertain of the diagnosis in the in-betweeners (30%)2 BNP Ventricular pressure & Stretch Pro-BNP Nt-BNP(spec) & BNP(sens)

Prospective, Blinded 1586 pts presenting with acute dyspnea ED Study Bedside assay Gold Standard = 2 cardiologists

Breathing Not Properly Breathing Not Properly ad Breathing Not Properly

Prospective diagnostic test evaluation 7 centers 1586 patients BNP blinded Gold Standard Cardiology Chart Review 97% certainty by ED physician

At 80% EP certainty Sens: 49% Specificity: 96% At 100 pg/ml Sens: 90% Specificity: 73% adf Breathing Not Properly Analysis BNP brings us closer to the gold standard Low Prob -EP

17% had CHF 90% would have been corrected by BNP High Prob -EP 4% did not have CHF 80% would have been corrected by BNP Uncertain -EP BNP correctly classified 74% Misclassified 7%

BNP Levels < 100 pg/ml may prompt clinician to focus on alternative diagnosis (COPD) Reasonable neg pred value Prognostic Value ?Variation with Age/Gender/Kidney fxn Prospective, Randomized, Controlled

Single blind 452 Pts with dyspnea Diagnostic Strategy (BNP) vrs Standard Assessment Told EP if <100 CHF unlikely, >500 CHF likely, 100-500 indeterminate End Points: Time to D/C & Total Cost Safety: Similar Conclusion: BNP improved evaluation thereby improving time to D/C and cost no change in safety

BNP strong prognostic indicator in symptomatic and asymptomatic individuals Death or Cardiac Death Additive to LVEF Cardiomyopathy http://www.medmovie.com/mmdat abase/MedMovieRedirect.aspx?Clie ntID=27

Case Previously well 10 year old girl presents with 2 weeks of progressive right sided ABD pain. General malaise. Mild fatigue on exertion. Parents report mild lethargy, pallor and decreased PO intake over same period. Shallow rapid breathing, worse when reclining at night.

37.8oC 123 24 94/54 Pale irritable HEENT: MMM. No adenopathy CVS: regular S1S2, no murmer, PPPx4, no edema CHEST: AE=AE slight decrease at bases ABD: palpable liver edge below umbilicus

EKG: sinus tach, LAD, flattened T-waves, decreased voltages. Post Myocarditis Dilated Cardiomyopathy Most common CM 30% idiopathic Hereditary

X-linked (dystrophin gene)

Booze Heavy Metal Drugs Infectious Viral Chagas Post partum Collagen vascular disease Glycogen storage disease Thiamine, PO4, zinc deficiency

Amyloidosis Neuromuscular disorders Dilated Cardiomyopathy Biopsy helpful for etiology Rx same as other CHF MDC (Metoprolol in Dilated CM) 34% reduction in Death Multicenter Myocarditis Treatment Trial no benefit of corticosteroids and

azathioprine for Rx of biopsy-proven inflammation in dilated CM HCM Inappropriate hypertrophy w/o stimulus Usually asymmetric 4% mortality per year (sudden death) HCM 50% familial (Dominant Inheritance) Mechanism

Abn Ca++ kinetics Abn sympathetic stim Abn Coronaries Subendocardial ischemia Structural abn

HCM 25% 1st relatives of HCM Usually 3rd decade not always M>F HCM - Presentation

Sudden Death Dysrhythmia CHF Presyncope / Syncope Angina HCM CHF Sx OE:

JVP prominent a wave Double impulse pulse PMI laterally displaced and increased SEM / HSM Split S2 HCM Genetic Studies ECG Echo LV outflow gradient >50mmHg

Diastolic dysfunction HOCM: septum >1.4:1 ratio to post wall HCM Approach/Mgmt

ABCD Normal CHF / CAD Rx Myomectomy Catheter septal ablation MV replacement ICD B-blockade CCB

Anti-arrhythmias Restrictive Least common CM Incidence likely under diagnosed Poor prognosis Cardiomyopathy http://www.medmovie.com/mmdat abase/MedMovieRedirect.aspx?Clie ntID=27

Restrictive Idiopathic restrictive cardiomyopathy EndoMyocardial Fibrosis Loeffler eosinophilic endomyocardial disease Secondary restrictive cardiomyopathy

Radiation Hemochromatosis Amyloidosis Scleroderma Carcinoid heart disease Glycogen storage disease of the heart Diagnosis

Chest x-ray Absence of cardiomegaly, normal cardiac silhouette CHF Electrocardiogram

LBBB common, RBBB possible Low voltage Nonspecific ST-T changes Various arrhythmias Chamber enlargement Echocardiography Normal to symmetrically thickened walls Rapid early-diastolic filling, slow latediastolic filling

Normal or slightly reduced ventricular volume and systolic function Cardiac catheterization Elevated ventricular end-diastolic pressure Dip and plateau configuration of the diastolic portion of the ventricular pressure pulse Normal to slightly decreased ejection fraction Prominent x and y descent

Endomyocardial biopsy May detect typical eosinophil infiltration in the inflammatory stage May detect myocardial fibrosis in later-stage cases Negative findings do not exclude diagnosis Treat underlying cause if possible Therapy similar for other causes of CHF Consider anticoagulation as prone to

stasis thromboembolism Thanks Shawn for the resources! References 1. 2. Kostuk WJ. Congestive heart failure: what can we offer our patients? CMAJ 2001;165(8):1053-5

Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med 2004;11:686-91. Risk of HF after AMI Jackson, G et al. BMJ 2000;320:167-170 Copyright 2000 BMJ Publishing Group Ltd. 20 pts Pulmonary Edema

Looked like needed intubation 2 intubated Also had COPD Mean Treatment Duration 2 h

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